The Role of NF-κB in Intracranial Aneurysm Pathogenesis: A Systematic Review

Intracranial aneurysms (IAs) are abnormal dilations of the cerebral vessels, which pose a persistent threat of cerebral hemorrhage. Inflammation is known to contribute to IA development. The nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-kappa B) is the major driver of inflammation. It increases the expression of inflammatory markers and matrix metalloproteinases (MMPs), which contribute heavily to the pathogenesis of IAs. NF-kappa B activation has been linked to IA rupture and resulting subarachnoid hemorrhage. Moreover, NF-kappa B activation can result in endothelial dysfunction, smooth muscle cell phenotypic switching, and infiltration of inflammatory cells in the arterial wall, which subsequently leads to the initiation and progression of IAs and consequently results in rupture. After a systematic search, abstract screening, and full-text screening, 30 research articles were included in the review. In this systematic review, we summarized the scientific literature reporting findings on NF-kappa B's role in the pathogenesis of IAs. In conclusion, the activation of the NF-kappa B pathway was associated with IA formation, progression, and rupture.

Automated summary

This systematic review examines the role of NF-kappa B in the pathogenesis of intracranial aneurysms (IAs), finding that its activation is closely associated with the formation, progression, and rupture of IAs.